Microglial activation in presymptomatic Huntington's disease gene carriers
Abstract
Microglial activation may play a role in the pathogenesis of Huntington's disease (HD). Using 11C-(R)-PK11195 (PK) positron emission tomography (PET), we investigated microglial activation in HD presymptomatic gene carriers (PGCs), its relationship with striatal neuronal dysfunction measured with 11C-raclopride (RAC) PET, and the role of PK PET as a possible marker of subclinical disease progression in PGCs. Eleven HD PGCs underwent PK and RAC PET. Their results were compared with those of healthy controls. PK and RAC binding was measured using region-of-interest analysis. Regional increases in PK binding were also localized with voxel-based statistical parametric mapping. HD PGCs had lower striatal RAC binding than the controls but significantly higher striatal and cortical PK binding. Individual levels of higher striatal PK binding in PGCs correlated with lower striatal RAC binding and, after excluding one outlier, with a higher probability of developing HD in 5 years. The inverse association between striatal PK and RAC binding in PGCs continues into early to moderate stages of HD. This study demonstrated for the first time in vivo widespread microglial activation in preclinical HD which correlated with striatal neuronal dysfunction. These findings indicate that microglial activation is an early event in the pathogenic processes of HD and is associated with subclinical progression of disease. PK PET may be a useful marker of active subclinical disease and a means of investigating the efficacy of neuroprotection strategies in PGCs.
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PET studies in presymptomatic Huntington disease gene carriers show increased microglial activation that correlates with striatal neuronal dysfunction.
“Positron emission tomography (PET) studies in presymptomatic HD gene carriers showed increased microglial activation, which correlated with striatal neuronal dysfunction (164).”
From Microglia Function in the Central Nervous System During Health and Neurodegeneration (2017) · cites this paper as [164]
11C(R)-PK11195 PET detected microglial activation in HD patients even before the onset of clinical symptoms.
“11C(R)-PK11195 PET detected microglial activation in HD patients even before the onset of clinical symptoms.”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [443]
Huntington's disease involves a reactive microglial response and inflammation.
“Huntington's disease is associated with a reactive microglial response and consequent inflammation.”
From Microglial depletion prevents extracellular matrix changes and striatal volume reduction in a model of Huntington's disease (2020) · cites this paper as Tai et al., 2007
In Huntington's disease, microglial activation is detected years before clinical symptom onset and correlates with striatal neuron dysfunction in subclinical and clinical stages.
“In Huntington's disease, microglial activation is detected years before the onset of clinical symptoms and correlates with striatal neuron dysfunction in subclinical (Tai et al. , 2007) as well as clinical stages of the disease (Pavese et al. , 2006; Politis et al. , 2011).”
From Microglial depletion prevents extracellular matrix changes and striatal volume reduction in a model of Huntington's disease (2020) · cites this paper as Tai et al., 2007
Dysregulation of microglia functions contributes to the pathogenesis of neurodegenerative diseases including Alzheimer's disease, Parkinson's disease and Huntington's disease.
“Dysregulation of microglia functions contribute to the pathogenesis of neurodegenerative diseases, including Alzheimer’s disease (AD) (6–8), Parkinson’s disease (PD) (9–12) and Huntington’s disease (HD) (13–15).”
From An environment-dependent transcriptional network specifies human microglia identity (2017) · cites this paper as [15]
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- Authors
- Tai, Y. F., Pavese, N., Gerhard, A., Tabrizi, S. J., Barker, R. A., Brooks, D. J., & Piccini, P.
- Affiliations
- Hammersmith Hospital (GB)
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2007-05-29
- Volume
- 130
- Issue
- 7
- Pages
- 1759-1766
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- OpenAlex
- W1992898455
- Cited by
- 440
- References
- 33
- Citations by year
- 2026: 13 · 2025: 16 · 2024: 28 · 2023: 27 · 2022: 16 · 2021: 31 · 2020: 30 · 2019: 22 · 2018: 22 · 2017: 29 · 2016: 27 · 2015: 25 · 2014: 31 · 2013: 16 · 2012: 20
- FWCI
- 8.63
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Research Explorer (The University of Manchester) (submittedVersion)
- Funders
- Wellcome Trust (GR071659AIA)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological diseases and metabolism
- Keywords
- Huntington's disease, microglial activation, [11C]PK11195 PET, [11C]raclopride PET, neurodegeneration biomarkers, neuroprotection
- MeSH terms
- Adult, Brain Mapping, Carbon Radioisotopes, Cerebral Cortex, Corpus Striatum, Female, Heterozygote, Humans, Huntington Disease, Image Processing, Computer-Assisted, Isoquinolines, Male, Middle Aged, Neurons, Microglia, Disease Progression, Radiopharmaceuticals, Raclopride, Positron-Emission Tomography
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